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Myonectin inhibits adipogenesis in 3T3-L1 preadipocytes by regulating the p38 MAPK pathway
Tae-Jun Park1,3,# (Graduate student), Anna Park2,3,# (Graduate student), Jaehoon Kim2 (Professor), Jeong-Yoon Kim1 (Professor), Baek Soo Han3 (Professor), Kyoung-Jin Oh3 (Professor), Eun Woo Lee3 (Professor), Sang Chul Lee3 (Professor), Kwang-Hee Bae3 (Professor), Won Kon Kim3,* (Professor)
1Department of Microbiology and Molecular Biology, Chungnam National University,
2Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST),
3Metabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
Today, obesity is a major health problem, which is closely associated with metabolic diseases such as diabetes, dyslipidemia, and cardiovascular disease. The direct cause of obesity is known as an abnormal increase in fat cell size and the adipocyte pool. Hyperplasia, in which the number of adipocytes increase, is closely related to adipogenesis in which preadipocytes differentiate into mature adipocytes. Adipogenesis is done with systematic signaling transduction by the expression of adipogenic transcription factors. Therefore, the regulation of adipogenesis is an important target for preventing obesity. Myonectin, a member of the CTRP family, is a type of myokine released by skeletal muscle cells. Although several studies have shown that myonectin is associated with lipid metabolism, the role of myonectin in the adipogenesis process is not known. Here, we demonstrate the role of myonectin during the differentiation of 3T3-L1 cells. We found that myonectin inhibits the adipogenesis of 3T3-L1 preadipocytes with a reduction in the expression of adipogenic transcription factors such as C/EBPメ, モ and PPARャ. Furthermore, we show that myonectin has an inhibitory effect on adipogenesis through the regulation of the p38 MAPK pathway and CHOP. These findings suggest that myonectin could potentially be used as a new therapeutic target to prevent obesity.
Abstract, Accepted Manuscript(in press) [Submitted on November 26, 2020, Accepted on December 4, 2020]
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